Human physiological signals are perpetual. These signals are spontaneous or induced with molecular, cellular chemical, and/or neural origins. Many of these physiological signals manifest themselves in motions in order to perform biologic and biochemical functions that sustain life. The better known motions are heartbeats, respiration, and cardiopulmonary functions. But there are far subtler motions in all parts of a human body necessary and essential to support life. These physiological motions have been shown to follow certain non-linear dynamic laws and possess fractal features and entrainment properties. These physiological motions are related to demographic factors, for example, gender and age, and closely associated with the health or disease conditions of a human body. Physiological dynamics, while not always seen or felt by humans, are nonetheless always present and essential to life.
In particular, these constant physiological motions are present in the entire cardiovascular and circulatory system including arteries, veins, and capillaries. Vasculature motions include vasomotion, vasodilation, vasoconstriction, and vasospasm. These spontaneous motions in the vasculature system also lead to rhythmic changes in vessel diameter, wall thickness, and vessel distensibility. Furthermore, blood vessels are elastic and characterized by certain viscoelastic properties. The dynamic and elastic nature of the vessels has particular effects on the success or failure of a therapeutic cardiovascular device.
Percutaneous access for various cardiovascular interventions is considered a safer and less invasive alternative to surgery. This procedure was developed in early 1950's and has since evolved into a popular and useful procedure treating a wide range of cardiovascular and vascular diseases including abdominal aortic aneurysm and heart valve repairs. Percutaneous access is either diagnostic or interventional (for example, percutaneous coronary intervention or PCI) with several possible access sites including access through an artery or a vein (for example, femoral, radial, or brachial), or transapical access. Each access site has its advantages and limitations. The choice of the access site is dependent on the disease condition and certain relevant clinical factors. But the choice can also be the preference of a practicing interventional cardiologist or radiologist. In all of these percutaneous interventions, there is a common denominator, that is, hemostasis and healing of the vascular wound.
The access site preference in percutaneous procedures has evolved over time and is currently geographically stratified. Today, the angioplasty procedure in the US is >95% transfemoral while transradial access is favored in Europe and Asia at approximately 70%. In the US, there has been a surge of radial access since 2007, mainly in response to the unabated bleeding and medical complications associated with the transfemoral access. Reducing femoral bleeding complications is cited as the sole reason for converting to radial access, even though radial access has its own limitations and disadvantages. Despite unabated bleeding medical events, femoral access is unlikely to be fully replaced because of its certain clinical advantages. Successful access site hemostasis and subsequent wound healing is important by itself as bleeding complications are associated not only with serious human costs including fatality, amputation, life-long pain, and disability, but also with significant healthcare expenditures in managing bleeding complications. Proper hemostasis and healing of the access site wound is an integral component to the underlying intervention, as it either contributes to the success of, or compromises, the intervention.
Traditional designs of hemostasis devices for percutaneous access site are based on the mechanistic barrier concept of treating the “hole” of the injured vessel more like a hole in a leaking water pipe, that is, a leaking water pipe which is rigid and stationary with constant dimensions. This barrier concept is reflected by many conventional terms such as “seal”, “plug”, or “clamping”. As a means to cause hemostasis, the implant device provides a physical barrier to “plug” or “seal” a vascular “hole”, while the current topical devices provide a mechanical barrier to “clamp” an injured vessel to stop outward blood flow. In reality, these sealing and clamping actions only provide a resistive force to resist blood, particularly resisting high velocity arterial blood from gushing out upon sheath removal. These actions do not cause hemostasis as defined by the completion of a cascade of time-dependent cellular processes of platelet aggregation, fibrin matrix formation, and subsequent wound healing phases. Moreover, blood vessels are not a rigid stationary structure. Instead, blood vessels are soft, elastic, and in various modes of perpetual motions and constantly changing vessel diameter, wall thickness, and tone.
The nature of the dynamic and elastic injury site explains why a precisely fitted implant may be disoriented or dislocated after seemingly initial hemostasis success and why precise topical clamping can still cause bleeding to turn internal or cause hematoma to form outside of the access location. The concept of plugging or clamping a “hole” in a rigid and stationary structure is not applicable to human vessel systems. Furthermore, an injury in a human body, even if local or perceived as local, is far from being localized, and is connected to and affected by, and also affects, the surrounding anatomical structures in both known and unknown manners. Managing the injured vessel “hole” must take a broader view beyond the injury site. In addition, the anatomy and the surrounding vascular and musculoskeletal structures at the femoral site are far more complex and significantly different from that at the radial site. But the current barrier concept does not differentiate between the two and rely on the same clamping mechanism to clamp the “same (radial or femoral) hole” of an injured vessel.
It is well documented that the initial seemingly successful hemostasis on the skin puncture surface can turn into a serious bleeding medical event later in an unpredictable way. The timeframe for delayed hemostasis breach is from hours to days, and in rare cases, months. And it can manifest in several forms including life-threatening “invisible” retroperitoneal bleeding or hematoma formed at location(s) other than the access site. These well-known clinical observations signify that the bleeding direction is not limited to the skin puncture surface as commonly perceived, and further validate that the “hole” is not a stationary structure. To date, there have been no effective answers to these clinical observations, nor an effective way to predict, thus prevent, delayed hemostasis breach.
There are two types of topical hemostasis devices currently on the market to manage bleeding at the access site. One is a “topical patch”, applied over the skin puncture site where the manufacturer claims to stop bleeding faster by visually judging no blood oozing out on the skin puncture surface. The other is the equivalent of manual compression, that is, by providing a compression force with a mechanical device. The former (topical patch) provides a false sense of hemostasis as the injury is the breached vessel under the skin and the skin surface hemostasis is not an indication of true and sustainable hemostasis. Nor does the latter (manual or device compression) solve the problem. In fact, an exhaustive scientific literature search has shown that compression pressure either at the vascular level, or at the skin level, does not cause platelet aggregation and fibrin formation. Furthermore, a strong and prolonged compression is known to hinder cellular coagulation and cause additional injury and neurological damage to the patient.
By relying on the barrier concept, access site bleeding complications, particularly at the anatomically more complex femoral site, remain unabated after more than half a century. In the meantime, advances in percutaneous technique have led to more complex interventions requiring larger catheter size (for example, 24 F in certain interventions) and more aggressive use of anticoagulants, both of which are known risk factors of bleeding complications. In spite of significant evolutions in percutaneous techniques, manual compression remains today the “gold standard” in managing access site hemostasis, even though ample clinical experiences and large scale statistics have confirmed that manual compression is inadequate and inapplicable in many situations. Today, access site bleeding and vascular complications remain a significant medical and economic issue decades after the advent of the percutaneous procedure. A safe and rigorous clinical solution to manage access site bleeding would improve patient safety and contribute to advancing the percutaneous technique.